RBCCNSDietG6PG6P GLY HEPATOADIPOSKM2,4,5 11 2,3 2,4,5 8 7,82,4,52,3,4,5 6 G6P G6P G3G1 1 1 1 G2 G4-mG4-mG4-m ATP A. Digestive Phase ATP ATP TG G’OL3P G6P TG GlucoseATP 6 ATP GLY ATP G6P AAs G’OL ATP ATP13 TG 11 11 12 12 FFA A,4,5 GLY ATP RBCSKMG6P KBs CNS2,4,5112 3 HEPATOFFA 9 11 10 KBs A,4,5 A,4,5 B,4,5 G4-iG4-i B,4,5 ADIPOB,4,5 GLY G6P LACT ATP G6P Glucose PROT G4-iG4-i G1G1 G3G3 G2G2 B. Fasting Phase •Fig. 39.3 A, Overview of glucose utilization during the digestive phase. GLUTtransporters:G1,GLUT1;G2,GLUT2;G3,GLUT3;G4-m,functionalGLUT4localizedtocellmembrane.Celltypes:ADIPO,adipocyte;CNS,centralnervoussystemneuronsandglia;HEPATO,hepatocyte;RBC,redbloodcell;SKM,skeletalmyocyte.Metabolites:G6P,glucose-6-phosphate;GLY,glycogen;G’OL3P,glycerol-3-phosphate;TG,triglyceride.Metabolicreactions/pathways:1,hexokinase/glucokinase;2,glycolysis;3,lactatedehydrogenase;4,TCAcycle± pyruvatedehydrogenase;5,oxidativephosphorylation;6,glycogensynthesis;7,denovolipogenesis;8,esterificationofFFAstoG’OL3PtoformTG.B, Overview of energy metabolism during the fasting phase. GLUTtransporters:seelegendforA,plus:G4-I,inactiveGLUT4withintracellularlocalization.Celltypes:seelegendforAMetabolites:seelegendforA,plus:AAs,aminoacids;FFA,freefattyacid;G’OL,glycerol;KBs,ketonebodies;LACT,lactate;PROT,protein.Metabolicreactions/pathways:seelegendforA,plus:9,glycogenolysis;10,gluconeogenesis;11,G6Pase;12,ketogenesis;13,proteolysis;A,β-oxidation;B,ketolysis.
and death) can occur. This means that whole-body metabolism during the interdigestive and fasting phases must meet the challenge of maintaining blood glucose above 60 mg/ dL (see
Fig. 39.2 , green arrow).
On the other hand, glucose levels must be maintained below a certain maximal threshold (i.e., fasting blood glucose < 100 mg/dL) to avoid glucose-induced side reactions (both enzymatic and nonenzymatic) as well as osmotic imbalances that lead to multiple forms of damage to cell function (see
Fig. 39.2 , red arrow).